Association of air pollution and green space with all-cause general practitioner and emergency room visits: A cross-sectional study of young people and adults living in Belgium.

BACKGROUND: Residing in areas with lower levels of air pollution and higher green space is beneficial to physical and mental health. We investigated associations of PM2.5, tree cover and grass cover with in-hours and out-of-hours GP visits and ER visits, for young people and adults. We estimated potential cost savings of GP visits attributable to high PM2.5. METHODS: We linked individual-level health insurance claims data of 315,123 young people (10-24 years) and 885,988 adults (25-64 years) with census tract-level PM2.5, tree cover and grass cover. Deploying negative binomial generalized linear mixed models, we estimated associations between quartile exposures and the three outcome measures. RESULTS: For in-hours and out-of-hours GP visits, among young people as well as adults, statistically significant pairwise differences between quartiles suggested increasing beneficial effects with lower PM2.5. The same outcomes were statistically significantly less frequent in quartiles with highest tree cover (>30.00%) compared to quartiles with lower tree cover, but otherwise pairwise differences were not statistically significant. These associations largely persisted in rural and urban areas. Among adults living in urban areas lower grass cover was associated with increased in-hours GP visits and ER visits. Assuming causality, reducing PM2.5 levels to the lowest quartile (4.91-7.49 µg/m³), among adults, 195,964 in-hours and 74,042 out-of-hours GP visits could be avoided annually. Among young people, 27,457 in-hours and 22,423 out-of-hours GP visits could be avoided annually. Nationally, this amounts to an annual potential cost saving of €43 million (€5.7 million in out-of-pocket payments and €37.2 million in compulsory health insurance). CONCLUSION: Higher ambient PM2.5 and lower tree cover show associations with higher non-urgent and urgent medical care utilization. These findings confirm the importance of reducing air pollution and fostering green zones, and that such policies may contribute positively to economic growth.

Short-Term exposure to ambient air pollution and onset of work incapacity related to mental health conditions.

The OECD estimates that greater work absenteeism is one of the main drivers behind the impact of air pollution on gross domestic product loss, but research linking air pollution with work absenteeism is scarce. With air pollution increasingly being linked to poor mental health, and poor mental health having become one of the main reasons for work absenteeism, we examined whether the onset of work incapacity related to mental health conditions is associated with short-term fluctuations in ambient black carbon (BC), nitrogen dioxide (NO2), ozone (O3), and particulate matter 2.5 (PM2.5), estimating the contributions of these pollutants jointly, while accounting for relative humidity, total solar radiation and temperature. We conducted a bidirectional time-stratified case-crossover study with daily air pollution estimates by municipality linked with 12 270 events of work incapacity related to mental health conditions in 2019 in Belgium. We ran single- and multi-pollutant conditional logistic regression models for three different exposure windows (lag 0, 0-1 and 0-2), considering potential confounding by relative humidity and total solar radiation. We observed positive associations between work incapacity related to mental health conditions and BC, NO2, and O3 exposure, but findings for PM2.5 were inconsistent. Results from multi-pollutant models showed a 12% higher risk of work incapacity for an IQR increase in NO2 and O3 at the day of the event (lag 0), with estimates increasing to about 26% for average concentrations up to two days before the event (lag 0-2). We found evidence for effect modification by age and season in the association with NO2, with highest effect estimates in the age group 40-49 years and in spring and summer. For O3, we observed effect modification by type of mental health problem. This country-wide study suggests that air pollution aggravates within 48 h a likely existing propensity to enter work incapacity because of mental health conditions.

Impact of COVID-19-related public containment measures on the ST elevation myocardial infarction epidemic in Belgium: a nationwide, serial, cross-sectional study.

AIMS: The current study assessed the impact of COVID-19-related public containment measures (i.e. lockdown) on the ST elevation myocardial infarction (STEMI) epidemic in Belgium. METHODS AND RESULTS: Clinical characteristics, reperfusion therapy modalities, COVID-19 status and in-hospital mortality of consecutive STEMI patients who were admitted to Belgian hospitals for percutaneous coronary intervention (PCI) were recorded during a three-week period starting at the beginning of the lockdown period on 13 March 2020. Similar data were collected for the same time period for 2017-2019. An evaluation of air quality revealed a 32% decrease in ambient NO2 concentrations during lockdown (19.5 µg/m³ versus 13.2 µg/m³, p < .001). During the three-week period, there were 188 STEMI patients admitted for PCI during the lockdown versus an average 254 STEMI patients before the lockdown period (incidence rate ratio = 0.74, p = .001). Reperfusion strategy was predominantly primary PCI in both time periods (96% versus 95%). However, there was a significant delay in treatment during the lockdown period, with more late presentations (>12 h after onset of pain) (14% versus 7.6%, p = .04) and with longer door-to-balloon times (median of 45 versus 39 min, p = .02). Although the in-hospital mortality between the two periods was comparable (5.9% versus 6.7%), 5 of the 7 (71%) COVID-19-positive STEMI patients died. CONCLUSION: The present study revealed a 26% reduction in STEMI admissions and a delay in treatment of STEMI patients. Less exposure to external STEMI triggers (such as ambient air pollution) and/or reluctance to seek medical care are possible explanations of this observation.

Using Large-Scale NO2 Data from Citizen Science for Air-Quality Compliance and Policy Support.

Citizen science projects that monitor air quality have recently drastically expanded in scale. Projects involving thousands of citizens generate spatially dense data sets using low-cost passive samplers for nitrogen dioxide (NO2), which complement data from the sparse reference network operated by environmental agencies. However, there is a critical bottleneck in using these citizen-derived data sets for air-quality policy. The monitoring effort typically lasts only a few weeks, while long-term air-quality guidelines are based on annual-averaged concentrations that are not affected by seasonal fluctuations in air quality. Here, we describe a statistical model approach to reliably transform passive sampler NO2 data from multiweek averages to annual-averaged values. The predictive model is trained with data from reference stations that are limited in number but provide full temporal coverage and is subsequently applied to the one-off data set recorded by the spatially extensive network of passive samplers. We verify the assumptions underlying the model procedure and demonstrate that model uncertainty complies with the EU-quality objectives for air-quality monitoring. Our approach allows a considerable cost optimization of passive sampler campaigns and removes a critical bottleneck for citizen-derived data to be used for compliance checking and air-quality policy use.

Ambient Air Pollution-related Mortality in Dairy Cattle: Does It Corroborate Human Findings?

BACKGROUND: Despite insights for humans, short-term associations of air pollution with mortality to our knowledge have never been studied in animals. We investigated the association between ambient air pollution and risk of mortality in dairy cows and assessed effect modification by season. METHODS: We collected ozone (O3), particulate matter (PM10), and nitrogen dioxide (NO2) concentrations at the municipality level for 87,108 dairy cow deaths in Belgium from 2006 to 2009. We combined a case-crossover design with time-varying distributed lag models. RESULTS: We found acute and delayed associations between air pollution and dairy cattle mortality during the warm season. The increase in mortality for a 10 µg/m increase in 2-day (lag 0-1) O3 was 1.2% (95% confidence interval [CI] = 0.3%, 2.1%), and the corresponding estimates for a 10 µg/m increase in same-day (lag 0) PM10 and NO2 were 1.6% (95% CI = 0.0%, 3.1%) and 9.2% (95% CI = 6.3%, 12%), respectively. Compared with the acute increases, the cumulative 26-day (lag 0-25) estimates were considerably larger for O3 (3.0%; 95% CI = 0.2%, 6.0%) and PM10 (3.2%; 95% CI = -0.6%, 7.2%), but not for NO2 (1.4%; 95% CI = -4.9%, 8.2%). In the cold season, we only observed increased mortality risks associated with same-day (lag 0) exposure to NO2 (1.4%; 95% CI = -0.1%, 3.1%) and with 26-day (lag 0-25) exposure to O3 (4.6%; 95% CI = 2.2%, 7.0%). CONCLUSIONS: Our study adds to the epidemiologic findings in humans and reinforces the evidence on the plausibility of causal effects. Furthermore, our results indicate that air pollution associations go beyond short-term mortality displacement. (See video abstract at http://links.lww.com/EDE/B105.).

Small for gestational age and exposure to particulate air pollution in the early-life environment of twins.

Several studies in singletons have shown that maternal exposure to ambient air pollutants is associated with restricted fetal growth. About half of twins have low birth weight compared with six percent in singletons. So far, no studies have investigated maternal air pollution exposure in association with birth weight and small for gestational age in twins. We examined 4760 twins of the East Flanders Prospective Twins Survey (2002-2013), to study the association between in utero exposure to air pollution with birth weight and small for gestational age. Maternal particulate air pollution (PM10) and nitric dioxide (NO2) exposure was estimated using a spatial temporal interpolation method over various time windows during pregnancy. In the total group of twins, we observed that higher PM10 and NO2 exposure during the third trimester was significantly associated with a lower birth weight and higher risk of small for gestational age. However, the association was driven by moderate to late preterm twins (32-36 weeks of gestation). In these twins born between 32 and 36 weeks of gestation, birth weight decreased by 40.2g (95% CI: -69.0 to -11.3; p=0.006) and by 27.3g (95% CI: -52.9 to -1.7; p=0.04) in association for each 10µg/m³ increment in PM10 and NO2 concentration during the third trimester. The corresponding odds ratio for small for gestational age were 1.68 (95% CI: 1.27-2.33; p=0.0003) and 1.51 (95% CI: 1.18-1.95; p=0.001) for PM10 or NO2, respectively. No associations between air pollution and birth weight or small for gestational age were observed among term born twins. Finally, in all twins, we found that for each 10µg/m³ increase in PM10 during the last month of pregnancy the within-pair birth weight difference increased by 19.6g (95% CI: 3.7-35.4; p=0.02). Assuming causality, an achievement of a 10µg/m³ decrease of particulate air pollution may account for a reduction by 40% in small for gestational age, in twins born moderate to late preterm.

Prenatal Ambient Air Pollution, Placental Mitochondrial DNA Content, and Birth Weight in the INMA (Spain) and ENVIRONAGE (Belgium) Birth Cohorts.

BACKGROUND: Mitochondria are sensitive to environmental toxicants due to their lack of repair capacity. Changes in mitochondrial DNA (mtDNA) content may represent a biologically relevant intermediate outcome in mechanisms linking air pollution and fetal growth restriction. OBJECTIVE: We investigated whether placental mtDNA content is a possible mediator of the association between prenatal nitrogen dioxide (NO2) exposure and birth weight. METHODS: We used data from two independent European cohorts: INMA (n = 376; Spain) and ENVIRONAGE (n = 550; Belgium). Relative placental mtDNA content was determined as the ratio of two mitochondrial genes (MT-ND1 and MTF3212/R3319) to two control genes (RPLP0 and ACTB). Effect estimates for individual cohorts and the pooled data set were calculated using multiple linear regression and mixed models. We also performed a mediation analysis. RESULTS: Pooled estimates indicated that a 10-µg/m3 increment in average NO2 exposure during pregnancy was associated with a 4.9% decrease in placental mtDNA content (95% CI: -9.3, -0.3%) and a 48-g decrease (95% CI: -87, -9 g) in birth weight. However, the association with birth weight was significant for INMA (-66 g; 95% CI: -111, -23 g) but not for ENVIRONAGE (-20 g; 95% CI: -101, 62 g). Placental mtDNA content was associated with significantly higher mean birth weight (pooled analysis, interquartile range increase: 140 g; 95% CI: 43, 237 g). Mediation analysis estimates, which were derived for the INMA cohort only, suggested that 10% (95% CI: 6.6, 13.0 g) of the association between prenatal NO2 and birth weight was mediated by changes in placental mtDNA content. CONCLUSION: Our results suggest that mtDNA content can be one of the potential mediators of the association between prenatal air pollution exposure and birth weight. CITATION: Clemente DB, Casas M, Vilahur N, Begiristain H, Bustamante M, Carsin AE, Fernández MF, Fierens F, Gyselaers W, Iñiguez C, Janssen BG, Lefebvre W, Llop S, Olea N, Pedersen M, Pieters N, Santa Marina L, Souto A, Tardón A, Vanpoucke C, Vrijheid M, Sunyer J, Nawrot TS. 2016. Prenatal ambient air pollution, placental mitochondrial DNA content, and birth weight in the INMA (Spain) and ENVIRONAGE (Belgium) birth cohorts. Environ Health Perspect 124:659-665; http://dx.doi.org/10.1289/ehp.1408981.

Fetal growth and maternal exposure to particulate air pollution--More marked effects at lower exposure and modification by gestational duration.

While there is growing evidence that air pollution reduces fetal growth, results are inconclusive with respect to the gestational window of effect. We investigated maternal exposure to particulate matter (PM10) in association with birth weight and fetus growth with a focus on the shape of the association and gestational age at birth as a potential effect modifier. The study population consisted of 525,635 singleton live births in Flanders (Belgium) between 1999 and 2009. PM10 exposure at maternal residence was averaged over various time windows. We used robust linear and logistic regression to estimate the effect of PM10 on birth weight and small for gestational age (SGA). Segmented regression models were applied for non-linear associations. Among moderately preterm (32-36 weeks) and term (>36 weeks) births, we found significant lower birth weight for all studied time windows. The estimated reduction in birth weight for a 10 µg/m(3) increase in average PM10 during pregnancy was 39.0 g (95% confidence interval [CI]: 26.4, 51.5 g) for moderately preterm births and 24.0 g (95% CI: 20.9, 27.2g) for term births. The corresponding odds ratios for SGA were 1.19 (95% CI: 1.07, 1.32) and 1.09 (95% CI: 1.06, 1.12) respectively. Segmented regression models showed stronger effects of PM10 on fetal growth at lower concentrations. Maternal PM10 exposure was significantly associated with a reduction in fetal growth among term and moderately preterm births, with a tendency of stronger effects for the latter and a flattening out of the slope at higher PM10 concentrations.

In Utero Fine Particle Air Pollution and Placental Expression of Genes in the Brain-Derived Neurotrophic Factor Signaling Pathway: An ENVIRONAGE Birth Cohort Study.

BACKGROUND: Developmental processes in the placenta and the fetal brain are shaped by the same biological signals. Recent evidence suggests that adaptive responses of the placenta to the maternal environment may influence central nervous system development. OBJECTIVES: We studied the association between in utero exposure to fine particle air pollution with a diameter ≤ 2.5 µm (PM2.5) and placental expression of genes implicated in neural development. METHODS: Expression of 10 target genes in the brain-derived neurotrophic factor (BDNF) signaling pathway were quantified in placental tissue of 90 mother-infant pairs from the ENVIRONAGE birth cohort using quantitative real-time polymerase chain reaction. Trimester-specific PM2.5 exposure levels were estimated for each mother's home address using a spatiotemporal model. Mixed-effects models were used to evaluate the association between the target genes and PM2.5 exposure measured in different time windows of pregnancy. RESULTS: A 5-µg/m3 increase in residential PM2.5 exposure during the first trimester of pregnancy was associated with a 15.9% decrease [95% confidence interval (CI): -28.7, -3.2%, p = 0.015] in expression of placental BDNF at birth. The corresponding estimate for synapsin 1 (SYN1) was a 24.3% decrease (95% CI: -42.8, -5.8%, p = 0.011). CONCLUSIONS: Placental expression of BDNF and SYN1, two genes implicated in normal neurodevelopmental trajectories, decreased with increasing in utero exposure to PM2.5. Future studies are needed to confirm our findings and evaluate the potential relevance of associations between PM2.5 and placental expression of BDNF and SYN1 on neurodevelopment. We provide the first molecular epidemiological evidence concerning associations between in utero fine particle air pollution exposure and the expression of genes that may influence neurodevelopmental processes.

Serum levels of club cell secretory protein (Clara) and short- and long-term exposure to particulate air pollution in adolescents.

BACKGROUND: Studies in populations have shown that particulate air pollution is associated with changes in lung function in adolescents. OBJECTIVE: We investigated the effect of short- and long-term exposure to particulate matter (PM10) on the pulmonary health of adolescents, using serum lung club cell secretory protein (Clara) (CC16) as a biomarker for respiratory epithelium integrity. METHODS: We measured serum CC16 in 825 adolescents (57% girls, mean age: 15 years). Short-term and long-term exposure to ambient PM10 was estimated for each participant's home address using a kriging interpolation method. To explore the association between PM10 and serum CC16 we applied restricted cubic splines with 5 knots located at the 5th, 25th, 50th, 75th and 95th percentiles of the PM10 distribution. The explorative analyses showed a change in the slope of this association, after which a change-point analysis was performed. RESULTS: After adjustment for potential covariates, the analysis showed strong associations between PM10 concentrations, averaged over the week preceding the clinical examination, and serum CC16 levels. Each 5 µg/m(3) increase in mean PM10 concentration in the week before the clinical examination was associated with a substantial increase of 0.52 µg/l (95% confidence interval: 0.31 to 0.73; p<0.0001) in serum CC16 levels. The association appears nonlinear with a flattening out of the slope at mean week PM10 levels above 37 µg/m(3). There was no evidence of an association between long-term exposure to PM10 and serum CC16 concentrations. CONCLUSIONS: Our findings suggest that short-term exposure to particulate air pollution may compromise the integrity of the lung epithelium and lead to increased epithelial barrier permeability in the lungs of adolescents, even at low concentrations.

Influence of ambient air pollution on global DNA methylation in healthy adults: a seasonal follow-up.

BACKGROUND: DNA methylation changes are potential pathways of environmentally induced health effects. We investigated whether exposure to ambient concentrations of NO2, PM10, PM2.5 and O3 and traffic parameters were associated with global DNA methylation in blood of healthy adults. METHODS: 48 non-smoking adults (25 males) with a median age of 39years were sampled in winter and summer. Global DNA methylation in whole blood (% 5-methyl-2'-deoxycytidine, %5mdC) was analyzed with HPLC. Exposure to air pollutants at the home address was assessed using interpolated NO2, PM10, PM2.5 and O3 concentrations for various exposure windows (60- to 1-day moving average exposures and yearly averages) and GIS-based traffic parameters. Associations between pollutants and %5mdC were tested with multiple mixed effects regression models. RESULTS: Average %5mdC (SD) was 4.30 (0.08) in winter and 4.29 (0.08) in summer. Men had higher %5mdC compared to women both in winter (4.32 vs. 4.26) and summer (4.31 vs. 4.27). When winter and summer data were analyzed together, various NO2, PM10 and PM2.5 moving average exposures were associated with changes in %5mdC (95% CI) ranging from -0.04 (-0.09 to 0.00) to -0.14 (-0.28 to 0.00) per IQR increase in pollutant. NO2, PM10, PM2.5 and O3 moving average exposures were associated with decreased %5mdC (95% CI) varying between -0.01 (-0.03 to 0.00) and -0.17 (-0.27 to -0.06) per IQR increase in pollutant in summer but not in winter. CONCLUSION: Decreased global DNA methylation in whole blood was associated with exposure to NO2, PM10, PM2.5 and O3 at the home addresses of non- adults. Most effects were observed for the 5- to 30-day moving average exposures.

Placental DNA hypomethylation in association with particulate air pollution in early life.

BACKGROUND: There is evidence that altered DNA methylation is an important epigenetic mechanism in prenatal programming and that developmental periods are sensitive to environmental stressors. We hypothesized that exposure to fine particles (PM2.5) during pregnancy could influence DNA methylation patterns of the placenta. METHODS: In the ENVIRONAGE birth cohort, levels of 5'-methyl-deoxycytidine (5-mdC) and deoxycytidine (dC) were quantified in placental DNA from 240 newborns. Multiple regression models were used to study placental global DNA methylation and in utero exposure to PM2.5 over various time windows during pregnancy. RESULTS: PM2.5 exposure during pregnancy averaged (25th-75th percentile) 17.4 (15.4-19.3) µg/m3. Placental global DNA methylation was inversely associated with PM2.5 exposures during whole pregnancy and relatively decreased by 2.19% (95% confidence interval [CI]: -3.65, -0.73%, p = 0.004) for each 5 µg/m3 increase in exposure to PM2.5. In a multi-lag model in which all three trimester exposures were fitted as independent variables in the same regression model, only exposure to PM2.5 during trimester 1 was significantly associated with lower global DNA methylation (-2.13% per 5 µg/m3 increase, 95% CI: -3.71, -0.54%, p = 0.009). When we analyzed shorter time windows of exposure within trimester 1, we observed a lower placental DNA methylation at birth during all implantation stages but exposure during the implantation range (6-21d) was strongest associated (-1.08% per 5 µg/m3 increase, 95% CI: -1.80, -0.36%, p = 0.004). CONCLUSIONS: We observed a lower degree of placental global DNA methylation in association with exposure to particulate air pollution in early pregnancy, including the critical stages of implantation. Future studies should elucidate genome-wide and gene-specific methylation patterns in placental tissue that could link particulate exposure during in utero life and early epigenetic modulations.

Impact of air pollution on cystic fibrosis pulmonary exacerbations: a case-crossover analysis.

BACKGROUND: Pulmonary exacerbations in cystic fibrosis (CF) contribute to the burden of disease, with a negative impact on quality of life, costs, and lung function. Our aim was to evaluate whether exacerbations, defi ned by antibiotic use, were triggered by daily fl uctuations in air pollution. METHODS: In a case-crossover analysis, we evaluated 215 patients with CF and pollution data from January 1, 1998, to December 31, 2010. Exacerbation was defi ned as the start of IV or oral antibiotic use in a home or hospital setting. We calculated regional background levels of particulate matter with a diameter , 10 m m (PM 10 ), ozone, and nitrogen dioxide (NO 2 ) on the day of the event and on the 2 days prior to the event at each patient's home address. We matched for day of the week and controlled for temperature on the day of the event and the 2 preceding days. In the month where antibiotic treatment was started, all days with the same temperature ( 2°C) as the event day served as control days, excluding 3 days before and after the start of treatment. RESULTS: A total of 215 patients (male sex, 49%, mean age, 21 13 years) had 2,204 antibiotic treatments (1,107 IV and 1,097 oral). Over a period of 12 years, an increase in risk of antibiotic use was associated with increasing concentrations of PM 10 , NO 2 , and ozone on the event day and for NO 2 on the day before. A tendency toward signifi cance was seen the day before antibiotic use for PM 10 and ozone. Overall, a rise in OR was seen from 2 days before until the day of the start of antibiotics. CONCLUSIONS: In patients with CF and exacerbations, ambient concentrations of ozone, PM 10 , and NO 2 play a role in triggering an exacerbation.

Placental mitochondrial DNA content and particulate air pollution during in utero life.

BACKGROUND: Studies emphasize the importance of particulate matter (PM) in the formation of reactive oxygen species and inflammation. We hypothesized that these processes can influence mitochondrial function of the placenta and fetus. OBJECTIVE: We investigated the influence of PM10 exposure during pregnancy on the mitochondrial DNA content (mtDNA content) of the placenta and umbilical cord blood. METHODS: DNA was extracted from placental tissue (n = 174) and umbilical cord leukocytes (n = 176). Relative mtDNA copy numbers (i.e., mtDNA content) were determined by real-time polymerase chain reaction. Multiple regression models were used to link mtDNA content and in utero exposure to PM10 over various time windows during pregnancy. RESULTS: In multivariate-adjusted analysis, a 10-µg/m³ increase in PM10 exposure during the last month of pregnancy was associated with a 16.1% decrease [95% confidence interval (CI): -25.2, -6.0%, p = 0.003] in placental mtDNA content. The corresponding effect size for average PM10 exposure during the third trimester was 17.4% (95% CI: -31.8, -0.1%, p = 0.05). Furthermore, we found that each doubling in residential distance to major roads was associated with an increase in placental mtDNA content of 4.0% (95% CI: 0.4, 7.8%, p = 0.03). No association was found between cord blood mtDNA content and PM10 exposure. CONCLUSIONS: Prenatal PM10 exposure was associated with placental mitochondrial alterations, which may both reflect and intensify oxidative stress production. The potential health consequences of decreased placental mtDNA content in early life must be further elucidated.

Does air pollution trigger infant mortality in Western Europe? A case-crossover study.

BACKGROUND: Numerous studies show associations between fine particulate air pollutants [particulate matter with an aerodynamic diameter ≤ 10 µm (PM10)] and mortality in adults. OBJECTIVES: We investigated short-term effects of elevated PM10 levels on infant mortality in Flanders, Belgium, and studied whether the European Union (EU) limit value protects infants from the air pollution trigger. METHODS: In a case-crossover analysis, we estimated the risk of dying from nontraumatic causes before 1 year of age in relation to outdoor PM10 concentrations on the day of death. We matched control days on temperature to exclude confounding by variations in daily temperature. RESULTS: During the study period (1998-2006), PM10 concentration averaged 31.9 ± 13.8 µg/m³. In the entire study population (n = 2,382), the risk of death increased by 4% [95% confidence interval (CI), 0-8%; p = 0.045] for a 10-µg/m³ increase in daily mean PM10. However, this association was significant only for late neonates (2-4 weeks of age; n = 372), in whom the risk of death increased by 11% (95% CI, 1-22%; p = 0.028) per 10-µg/m³ increase in PM10. In this age class, infants were 1.74 (95% CI, 1.18-2.58; p = 0.006) times more likely to die on days with a mean PM10 above the EU limit value of 50 µg/m3 than on days below this cutoff. CONCLUSIONS: Even in an affluent region in Western Europe, where infant mortality is low, days with higher PM air pollution are associated with an increased risk of infant mortality. Assuming causality, the current EU limit value for PM10, which may be exceeded on 35 days/year, does not prevent PM10 from triggering mortality in late neonates.

Air pollution related prothrombotic changes in persons with diabetes.

BACKGROUND: Population studies suggest that persons with diabetes are more sensitive to the effects of particulate matter (PM) air pollution. However, the biological mechanisms of a possible prothrombotic effect underlying this enhanced susceptibility remain largely unknown. OBJECTIVE: We hypothesized that exposure to PM causes prothrombotic changes in persons with diabetes, possibly via systemic inflammation. METHODS: Our study included 137 nonsmoking adults with diabetes who were outpatients at the University Hospital Leuven. Recent exposure (2 hr before examination) to ambient PM was measured at the entrance of the hospital. Individual chronic exposure to PM was assessed by measuring the area occupied by carbon in airway macrophages obtained by sputum induction. Platelet function was measured ex vivo with the PFA-100 platelet function analyzer, which simulates a damaged blood vessel; we analyzed the function of platelets in primary hemostasis under high shear conditions. Total and differential blood leukocytes were counted. RESULTS: Independent of antiplatelet medication, an interquartile range (IQR) increase of 39.2 microg/m3 in PM10 (PM with aerodynamic diameter

Spatial interpolation of ambient ozone concentrations from sparse monitoring points in Belgium.

Due to scientific interest on the one hand and political and regulatory obligations on the other hand the monitoring of ozone in the troposphere is an important issue. To this end, in Belgium as in many other countries, a fixed network of monitoring stations is operated. In order to estimate the ozone concentrations over the whole territory, a model is needed to spatially complement the sparse measurements. This paper describes the development of an interpolation scheme which is aimed at fast operational use. The model uses the population density as auxiliary data to remove a spatial trend due to titration by nitric oxide. The residuals are interpolated by kriging. As a benchmark the inverse distance weighting interpolation method is used with and without the detrending. The proposed model systematically improves the interpolation and makes a significant difference when estimating human exposure to ozone. It is generic in design, easy to implement and flexible to changes in the monitoring network.